PMID- 33182035
OWN - NLM
STAT- MEDLINE
DCOM- 20210602
LR  - 20210602
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 88
DP  - 2020 Nov
TI  - 3,4,5-Trihydroxycinnamic acid exerts anti-asthmatic effects in vitro and in vivo.
PG  - 107002
LID - S1567-5769(20)32050-6 [pii]
LID - 10.1016/j.intimp.2020.107002 [doi]
AB  - 3,4,5-Trihydroxycinnamic acid (THCA) has been reported to possess 
      anti-inflammatory activity. However, the effect of THCA for treating allergic 
      asthma was unknown. Therefore, in the present study, the anti-asthmatic effects 
      of THCA were studied in both in vitro and in vivo studies. In phorbol 
      12-myristate 13-acetate (PMA)-stimulated A549 airway epithelial cells, THCA 
      pretreatment decreased the mRNA expression and secretion of interleukin (IL)-8, 
      monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecules 
      1 (ICAM-1), and reduced the mRNA expression of matrix metalloproteinase 9 
      (MMP-9). THCA also inhibited PMA-induced protein kinase B (AKT), 
      mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-kappaB) 
      activation in A549 cells. In lipopolysaccharide (LPS)-stimulated RAW264.7 
      macrophages, THCA pretreatment suppressed the mRNA expression of ICAM-1 and 
      MMP-9. In addition, THCA suppressed the adhesion of EOL and A549 cells. In 
      ovalbumin (OVA)-administered asthmatic mice, THCA exerted inhibitory activity on 
      IL-5, IL-13, and MCP-1 in bronchoalveolar lavage fluid (BALF) and on OVA-specific 
      immunoglobulin E (IgE) in serum. THCA attenuated the numbers of inflammatory 
      cells in BALF and the influx of inflammatory cell in lung tissues. Furthermore, 
      THCA downregulated the levels of inducible nitric oxide (iNOS), cyclooxygenase-2 
      (COX-2), and leukotriene B4 (LTB4) expression, mucus production and CREB 
      phosphorylation as well as Penh value. These effects were accompanied by 
      suppression of AKT, extracellular signal-regulated kinase (ERK), c-Jun N-terminal 
      kinase (JNK), and NF-kappaB activation. Therefore, the results of the current study 
      suggest that THCA may be a valuable adjuvant or therapeutic in the prevention or 
      treatment of allergic asthma.
CI  - Copyright (c) 2020 Elsevier B.V. All rights reserved.
FAU - Park, Ji-Won
AU  - Park JW
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea.
FAU - Kim, Seong-Man
AU  - Kim SM
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea; College of Pharmacy, 
      Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon 34134, Republic 
      of Korea.
FAU - Min, Jae-Hong
AU  - Min JH
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea; College of Pharmacy, 
      Chungbuk National University, Cheongju-si, Chungcheongbuk-do 28160, Republic of 
      Korea.
FAU - Kim, Min-Gu
AU  - Kim MG
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea; College of Pharmacy, 
      Chungbuk National University, Cheongju-si, Chungcheongbuk-do 28160, Republic of 
      Korea.
FAU - Kwon, Ok-Kyoung
AU  - Kwon OK
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea.
FAU - Hwang, Daseul
AU  - Hwang D
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea; College of Pharmacy, 
      Chungbuk National University, Cheongju-si, Chungcheongbuk-do 28160, Republic of 
      Korea.
FAU - Oh, Jae-Hoon
AU  - Oh JH
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea; College of Pharmacy, 
      Chungbuk National University, Cheongju-si, Chungcheongbuk-do 28160, Republic of 
      Korea.
FAU - Park, Min-Woo
AU  - Park MW
AD  - SciTech Korea Inc., Seoul 01138, Republic of Korea.
FAU - Chun, Wanjoo
AU  - Chun W
AD  - Department of Pharmacology, College of Medicine, Kangwon National University, 
      Chuncheon, Kangwon 24341, Republic of Korea.
FAU - Lee, Hee Jae
AU  - Lee HJ
AD  - Department of Pharmacology, College of Medicine, Kangwon National University, 
      Chuncheon, Kangwon 24341, Republic of Korea.
FAU - Kim, Doo-Young
AU  - Kim DY
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea.
FAU - Kim, Jung Hee
AU  - Kim JH
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea.
FAU - Hwang, Joonsung
AU  - Hwang J
AD  - Anticancer Agent Research Center, Korea Research Institute of Bioscience and 
      Biotechnology, (KRIBB), Chungbuk 28116, Republic of Korea.
FAU - Kim, Mun Ock
AU  - Kim MO
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea.
FAU - Oh, Sei-Ryang
AU  - Oh SR
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea.
FAU - Ahn, Kyung-Seop
AU  - Ahn KS
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea. Electronic address: 
      ksahn@kribb.re.kr.
FAU - Lee, Jae-Won
AU  - Lee JW
AD  - Natural Medicine Research Center, Korea Research Institute of Bioscience and 
      Biotechnology (KRIBB), Chungbuk 28116, Republic of Korea. Electronic address: 
      suc369@kribb.re.kr.
LA  - eng
PT  - Journal Article
DEP - 20200922
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (3,4,5-trihydroxycinnamic acid)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokines)
RN  - 0 (Cinnamates)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Animals
MH  - Asthma/*chemically induced/*drug therapy
MH  - Cell Adhesion/drug effects
MH  - Cell Adhesion Molecules/genetics/metabolism
MH  - Cell Line, Tumor
MH  - Chemokines/genetics/metabolism
MH  - Cinnamates/*pharmacology
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Macrophages/*drug effects
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Ovalbumin/toxicity
MH  - RAW 264.7 Cells
MH  - Random Allocation
OTO - NOTNLM
OT  - Allergic asthma
OT  - Eosinophil
OT  - ICAM-1
OT  - MMP-9
OT  - THCA
OT  - Th2 cytokines
COIS- Declaration of Competing Interest The authors declare that there are no conflicts 
      of interest.
EDAT- 2020/11/14 06:00
MHDA- 2021/06/03 06:00
CRDT- 2020/11/13 01:01
PHST- 2020/06/20 00:00 [received]
PHST- 2020/09/09 00:00 [revised]
PHST- 2020/09/09 00:00 [accepted]
PHST- 2020/11/14 06:00 [pubmed]
PHST- 2021/06/03 06:00 [medline]
PHST- 2020/11/13 01:01 [entrez]
AID - S1567-5769(20)32050-6 [pii]
AID - 10.1016/j.intimp.2020.107002 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2020 Nov;88:107002. doi: 10.1016/j.intimp.2020.107002. Epub 
      2020 Sep 22.